pharmacology Flashcards

1
Q

RANK

A

expressed on osteoclast precursor cells,

wen RANK activated, osteoclasts are activated

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2
Q

RANKL

A

expressed on osteoblasts.

these activate RANK on osteoclasts to activate osteoclasts =increase bone resroption

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3
Q

OPG

A

osteoprotegerin

soluble forms of RANK. mops up RANKL, stopping it from activating RANK i.e. bone protective

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4
Q

CALCITRIOL

A
  • active form of Vit D
  • Maintains Ca2+ in the plasma by increasing GIT uptake and decreasing renal exretion
  • AE: hypercalcemia (manifesting as nausea, vomiting, constipation, anorexia, sweating and polyuria)
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5
Q

CALCIUM

A

• Sucks by itself, give with other anti-resorptive agents eg calcitriol

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6
Q

SERM

A
  • Selective Estrogen Receptor Modulators
  • Drug: raloxifene
  • Modulates receptors on bone, increases estrogenic activity (oestrogen promotes bone mineralization), increases bone density.
  • AE: Venous thromboembolism.
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7
Q

BISPHOPHONATES

A
  • Drug: old/oral: alendronate (core drug), risedronate. New/intravenous: zoledronate, ibandronate
  • Firstline for post-menopausal women!

• MOA:
o Biphosphonates are analogs of pyrophosphate
o They are taken into bone, concentrated in bone, layed down in mineralized matrix of bone for many years-reducing rate of bone turnover.
o Also: reduce resorption of bone by inhibiting formation n activity of osteoclasts

• AE of biphosphonate generally:
o Osteonecrosis of jaw
o Atypical fractures (eg they are ok, bone density ok, no trauma ,but they suddenly present with pain froma hip fracture etc
o Anterolateral thigh pain

• AE of alendronate (core drug), risedronate
o GIT disturbances
o Ulceration – oesophagitis

• Complicated administrations for oral bisphosphonates

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8
Q

taking biphophonates

A
o	Take first dose early in the morning
• Take on an empty stomach
(30 min before food)
o	Separate administration of other
medications from bisphosphonate dose
• Swallow tablet whole –
do not crush, chew or suck
• Take with a full glass of water
• Patient to remain upright for 30 minutes to 1 hour after dose
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9
Q

DENOSUMAB

A
  • Monoclonal antibody against RANKL=decrease osteoclast activity
  • Used in postmenopausal women where bisphosphonates are unsuitable
  • Has negative immune systemic effects
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10
Q

CALCITONIN & SALCITONIN

A
  • inhibits osteoclasts activity, low efficacy

* calcitonin has (longer 1/2 life) than calcitonin

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11
Q

OESTROGEN/HORMONAL REPLACEMENT THERAPY

A
  • Increases OPG (decoy) thereby inhibiting osteoclasts.=inhibit bone loss
  • Aes: Increase risk of cancer and cardiovascular effects (not usually recommended).
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12
Q

BONE ANABOLIC AGENTS

A

PTH/PTH FRAGMENTS

STRONTIUM RANELATE

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13
Q

PTH/PTH FRAGMENTS

A
  • Drug: teriparatide
  • PTH segemtns mightseem contradictory, but if u give intermitteitnly by a dialy subcuuatnous regime., it actually causes bone anabolis (bone build up) n stimulatie osteobalst activey
  • Restricted use of 18mnth only in a pt’s lifetime. due to risk of osteosarcoma
  • used when high risk of fracture & other treatments unsuitable-later resort
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14
Q

STRONTIUM RANELATE

A
  • inhibits bone resorption, stimulates bone formation,
  • Increases OPG (decoy).
  • Decrease RANKL
  • Still in trials, question bout long term safety –seizrues, blood clots etc
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15
Q

metformin

A

first line for type 2 dm
increase tissue sensitivity to insulin
don’t give in pt with renal problem

SE: weight loss, nausea, diarrhoea

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16
Q

pioglitazone/rosiglitazone

class: glitazone/TZD

A

increase tissue sensitivity to insulin -bind to PPAR gamma

inhibit hepatic gluconeogenesis

SE: weight gain,
rosiglitazone - has issues with long term safety- CVD issues

17
Q

sulphonylureas

A

drug: glicazide
stimulate release of insulin by acting on pancreas cells

block ATP-sensitive K+ channels=cause depolarisation of beta cells=insulin released from cells.

SE: hypoglycaemia , weight gain (appetite stimulating), high protein binding

18
Q

glicazide

A

block ATP-sensitive K+ channels

the ORIGINAL

19
Q

glitinide

A

use if pt allergic to sulphon/glicazide
same MOA/job as glicazide/sulphonylureas
shorter duration of action to sulphon

20
Q

alpha glucosidase inhibitors

A

delay breakdown of carbo

carbo broken down to glucose by glucosides
drug= acarbose

21
Q

acarbose

A

delay breakdown of carbo by inhibiting glucosides
=helps with reducing the rising surge of blood glucose levels after a meal

SE= flatulance, diarrhoea

22
Q

exenatide

A

incretin mimetic

mimics effects of GLP-1

GLP-1 stimulates pancreas to release insulin wen we eat
=get initial rapid release of endogenous insulin

23
Q

sitagliptin

A

block DPP-4

DPP-4 is used to break down GLP-1 n GIP
=increase levels of GLP-1 n GIP

24
Q

GIP/GLP-1

A

stimulate pancreas to release insulin

25
Q

thionamides

A

drugs=carbimazole, propylthyrouracil

MOA: inhibit iodination of tyrosine on thyroglobulin =decrease T3, T4 synthesis

effects on apparent once uve depleted ur T3, T4 stores

Side effects: agranulocytosis, rashes (2 - 25%)
– headaches; nausea; jaundice; joint pains

carbimazole is the go to drug for hyperthyroidism- cos prop has hepatotoxicity
use propylthyrouracil in pregnancy (to prevent congenital hypothyroidsim- both carbim n propy can cross placenta decreasing thyroid hormones in baby, but carbim crosses more)

26
Q

high levels of iodine/iodide aka

/iodine/iodide supplementation

A

turns glands off -inhibit T3 T4 release
effects occur in 24 hrs n are short lasting (2wks)
↓ in vascularity and gland size (10-14 days): preparation for thyroidectomy

27
Q

radioactive iodine (131 I)

A

incorporated into thyroglobulin
emits cytotoxin beta particles wich kills thyroid cells-localised effect
contraindicated in pregnany n childhood/kids

AE: cancer, hypothyroidism

28
Q

T4

A

start with small dose in elderly in case of CVD issues

there mite be increased risk of osteoporosis

29
Q

T3`

A

used iv for speed of onset, e.g in myxoedema coma

30
Q

drugs affecting thyroid function

A

amiodarone
Iodinated Contrast media
kelp-seaweed